Journal
BLOOD
Volume 103, Issue 5, Pages 1909-1911Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2003-07-2577
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Funding
- NCI NIH HHS [CA21115, CA31946, CA68484, CA21765, CA101140, CA92551] Funding Source: Medline
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Aberrant expression of transcription factor oncogenes such as HOX11, HOX11L2, TAL1/SCL, LYL1, LMO1, and LMO2 can be detected in lymphoblasts from up to 80% of patients with acute T-cell lymphoblastic leukemia (T-ALL). Transcriptional activation of these oncogenes in leukemic cells typically results from chromosomal rearrangements that place them next to highly active cis-acting transcriptional regulatory elements. However, biallelic activation of TAL1 in some T-ALL cases has been previously proposed. We have used allele-specific mRNA analysis to show that trans-acting mechanisms leading to biallelic overexpression of TAL1 are involved in 10 (42%) of 24 TAL1(+) informative T-ALL cases, 2 (17%) of 12 HOX11(+) informative cases, and 7 (64%) of 11 LMO2(+) informative cases. We propose that aberrant expression of oncogenic transcription factors in a significant fraction of T-ALLs may result from loss of the upstream transcriptional mechanisms that normally down-regulate the expression of these oncogenes during T-cell development. (C) 2004 by The American Society of Hematology.
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